A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression. - Wikidata - awgldk - TriplyDB

A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression.

A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression.

http://www.wikidata.org/entity/Q30498959

about

Proteomics and biomarkers in clinical trials for drug development A Phase II Trial of AZD6244 (Selumetinib, ARRY-142886), an Oral MEK1/2 Inhibitor, in Relapsed/Refractory Multiple Myeloma MAF mediates crosstalk between Ras-MAPK and mTOR signaling in NF1.Curing myeloma at last: defining criteria and providing the evidence.The PP242 mammalian target of rapamycin (mTOR) inhibitor activates extracellular signal-regulated kinase (ERK) in multiple myeloma cells via a target of rapamycin complex 1 (TORC1)/eukaryotic translation initiation factor 4E (eIF-4E)/RAF pathway and Cytotoxic Properties of a DEPTOR-mTOR Inhibitor in Multiple Myeloma Cells.Dexamethasone-induced cell death is restricted to specific molecular subgroups of multiple myeloma.Aldehyde dehydrogenase-1a1 induces oncogene suppressor genes in B cell populations.Cytoplasmic calcium increase via fusion with inactivated Sendai virus induces apoptosis in human multiple myeloma cells by downregulation of c-Myc oncogene.Common genetic variants in 11q13.3 and 9q22.33 are associated with molecular subgroups of multiple myeloma TORC1 and class I HDAC inhibitors synergize to suppress mature B cell neoplasms.IκB kinase regulation of the TPL-2/ERK MAPK pathway.Molecular mechanisms of effectiveness of novel therapies in multiple myeloma.Understanding the molecular biology of myeloma and its therapeutic implications.MEK inhibitors as a chemotherapeutic intervention in multiple myeloma.Induction of immunoglobulin transcription factor 2 and resistance to MEK inhibitor in melanoma cells.IQGAP1 Scaffold-MAP Kinase Interactions Enhance Multiple Myeloma Clonogenic Growth and Self-Renewal.MAF protein mediates innate resistance to proteasome inhibition therapy in multiple myeloma.Relevance of the thyroid hormones-αvβ3 pathway in primary myeloma bone marrow cells and to bortezomib action.Combined targeting of MEK/MAPK and PI3K/Akt signalling in multiple myeloma.Therapeutic potential of MEK inhibition in acute myelogenous leukemia: rationale for "vertical" and "lateral" combination strategies.GSK3-mediated MAF phosphorylation in multiple myeloma as a potential therapeutic target Inhibiting MEK in MAPK pathway-activated myeloma.Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy.The AP-1 transcription factor JunB is essential for multiple myeloma cell proliferation and drug resistance in the bone marrow microenvironment.Active enhancer and chromatin accessibility landscapes chart the regulatory network of primary multiple myeloma.A TC classification-based predictor for multiple myeloma using multiplexed real-time quantitative PCR.The biological significance of histone modifiers in multiple myeloma: clinical applications

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A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression.

http://www.wikidata.org/entity/Q30498959

description

2010 nî lūn-bûn

@nan

2010 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

A mechanistic rationale for ME ...... de of MAF oncogene expression.

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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type

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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A mechanistic rationale for ME ...... de of MAF oncogene expression.

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Arthur L Shaffer

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Christina M Annunziata

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Elaine M Hurt

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Laurence Lamy

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Lidia Hernandez

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Lloyd T Lam

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Louis M Staudt

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R Eric Davis

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W Michael Kuehl

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P2860

Overexpression of transcripts originating from the MMSET locus characterizes all t(4;14)(p16;q32)-positive multiple myeloma patients

A subset of multiple myeloma harboring the t(4;14)(p16;q32) translocation lacks FGFR3 expression but maintains an IGH/MMSET fusion transcript

Overexpression of c-maf is a frequent oncogenic event in multiple myeloma that promotes proliferation and pathological interactions with bone marrow stroma

Cancer statistics, 2009

The regulation of AP-1 activity by mitogen-activated protein kinases

A loss-of-function RNA interference screen for molecular targets in cancer.

Identification of common predictive markers of in vitro response to the Mek inhibitor selumetinib (AZD6244; ARRY-142886) in human breast cancer and non-small cell lung cancer cell lines.

The molecular classification of multiple myeloma

The MMSET histone methyl transferase switches global histone methylation and alters gene expression in t(4;14) multiple myeloma cells.

Clinical experience of MEK inhibitors in cancer therapy.

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2396-2404

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